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Article: Potential Applications of Thyroid Hormone Derivatives in Obesity and Type 2 Diabetes: Focus on 3,5-Diiodothyronine (3,5-T2) in Psammomys obesus (Fat Sand Rat) Model

Bouazza, Asma / Favier, Roland / Fontaine, Eric / Leverve, Xavier / Koceir, Elhadj-Ahmed

Nutrients. 2022 July 25, v. 14, no. 15

2022

Abstract: 3,5-Diiodothyronine (3,5-T2) has been shown to exert pleiotropic beneficial effects. In this study we investigated whether 3,5-T2 prevent several energy metabolism disorders related to type 2 diabetes mellitus (T2DM) in gerbils diabetes-prone P. obesus. ... ...

Abstract	3,5-Diiodothyronine (3,5-T2) has been shown to exert pleiotropic beneficial effects. In this study we investigated whether 3,5-T2 prevent several energy metabolism disorders related to type 2 diabetes mellitus (T2DM) in gerbils diabetes-prone P. obesus. 157 male gerbils were randomly to Natural Diet (ND-controlled) or a HED (High-Energy Diet) divided in: HED- controlled, HED-3,5-T2 and HED- Placebo groups. 3,5-T2 has been tested at 25 µg dose and was administered under subcutaneous pellet implant during 10 weeks. Isolated hepatocytes were shortly incubated with 3,5-T2 at 10⁻⁶ M and 10⁻⁹ M dose in the presence energetic substrates. 3,5-T2 treatment reduce visceral adipose tissue, prevent the insulin resistance, attenuated hyperglycemia, dyslipidemia, and reversed liver steatosis in diabetes P. obesus. 3,5-T2 decreased gluconeogenesis, increased ketogenesis and enhanced respiration capacity. 3,5-T2 potentiates redox and phosphate potential both in cytosol and mitochondrial compartment. The use of 3,5-T2 as a natural therapeutic means to regulate cellular energy metabolism. We suggest that 3,5-T2 may help improve the deleterious course of obesity and T2DM, but cannot replace medical treatment.
Keywords	Psammomys obesus ; adipose tissue ; cytosol ; energy metabolism ; fatty liver ; gluconeogenesis ; hepatocytes ; high energy diet ; hyperglycemia ; hyperlipidemia ; insulin resistance ; males ; medical treatment ; mitochondria ; models ; noninsulin-dependent diabetes mellitus ; obesity ; phosphates ; placebos ; rats ; sand ; thyroid hormones
Language	English
Dates of publication	2022-0725
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2518386-2
ISSN	2072-6643
ISSN	2072-6643
DOI	10.3390/nu14153044
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Potential Applications of Thyroid Hormone Derivatives in Obesity and Type 2 Diabetes: Focus on 3,5-Diiodothyronine (3,5-T2) in

Bouazza, Asma / Favier, Roland / Fontaine, Eric / Leverve, Xavier / Koceir, Elhadj-Ahmed

Nutrients

2022 Volume 14, Issue 15

Abstract	3,5-Diiodothyronine (3,5-T2) has been shown to exert pleiotropic beneficial effects. In this study we investigated whether 3,5-T2 prevent several energy metabolism disorders related to type 2 diabetes mellitus (T2DM) in gerbils diabetes-prone
MeSH term(s)	Animals ; Diabetes Mellitus, Type 2/drug therapy ; Diabetes Mellitus, Type 2/metabolism ; Diiodothyronines ; Disease Models, Animal ; Gerbillinae ; Insulin/therapeutic use ; Male ; Obesity/drug therapy ; Obesity/metabolism ; Thyroid Hormones
Chemical Substances	Diiodothyronines ; Insulin ; Thyroid Hormones ; 3,5-diiodothyronine (534-51-0)
Language	English
Publishing date	2022-07-25
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2518386-2
ISSN	2072-6643 ; 2072-6643
ISSN (online)	2072-6643
ISSN	2072-6643
DOI	10.3390/nu14153044
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Article: Time course of the development of non-alcoholic hepatic steatosis in response to high-fat diet-induced obesity in rats.

Gauthier, Marie-Soleil / Favier, Roland / Lavoie, Jean-Marc

The British journal of nutrition

2005 Volume 95, Issue 2, Page(s) 273–281

Abstract: The aim of the study was to characterize the time course of the development of high-fat diet-induced hepatic steatosis and its relation to body fat accretion and changes in plasma lipid profile. Female Sprague-Dawley rats were high-fat fed (HF; 42 %, kJ) ...

Abstract	The aim of the study was to characterize the time course of the development of high-fat diet-induced hepatic steatosis and its relation to body fat accretion and changes in plasma lipid profile. Female Sprague-Dawley rats were high-fat fed (HF; 42 %, kJ) for 1, 2, 4, 6, 12 and 16 weeks and compared to standard fed rats (SD). Data obtained from HF rats were further analysed by classifying the animals into obesity-prone and obesity-resistant. In HF rats, liver lipid content increased rapidly by approximately 200 % during the first 2 weeks, decreased almost to baseline levels between weeks 2 and 6, and re-increased by 17 % between weeks 6 and 16 (P<0.05). Body weight, body fat accretion, plasma leptin, NEFA and glycerol concentrations were higher in HF than in SD rats (P<0.05). These higher values were established in 2 weeks and the differences between the groups did not further enlarge from weeks 2 to 16. Obesity-prone rats depicted higher body weight and body fat accretion than obesity-resistant and SD rats. Surprisingly, however, liver lipid content was the same in obesity-prone as in obesity-resistant rats as they were both higher than in SD rats (weeks 2 and 16; P<0.05). Our data support the hypothesis that the liver acts as a systemic buffer, largely increasing its lipid content in the early stage of high-fat feeding. Our results also suggest that the development of non-alcoholic hepatic steatosis is more linked to dietary fat ingestion than to body weight gain.
MeSH term(s)	3-Hydroxybutyric Acid/blood ; Adipose Tissue/metabolism ; Animals ; Diet ; Dietary Fats/administration & dosage ; Dietary Fats/analysis ; Energy Intake/physiology ; Fatty Acids, Nonesterified/blood ; Fatty Liver/blood ; Fatty Liver/etiology ; Female ; Glycerol/blood ; Leptin/blood ; Lipids/analysis ; Liver/metabolism ; Obesity/etiology ; Obesity/metabolism ; Rats ; Rats, Sprague-Dawley ; Time Factors ; Triglycerides/analysis ; Weight Gain/physiology
Chemical Substances	Dietary Fats ; Fatty Acids, Nonesterified ; Leptin ; Lipids ; Triglycerides ; Glycerol (PDC6A3C0OX) ; 3-Hydroxybutyric Acid (TZP1275679)
Language	English
Publishing date	2005-10-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	280396-3
ISSN	1475-2662 ; 0007-1145
ISSN (online)	1475-2662
ISSN	0007-1145
DOI	10.1079/bjn20051635
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Article: Prevention of unloading-induced atrophy by vitamin E supplementation: links between oxidative stress and soleus muscle proteolysis?

Servais, Stéphane / Letexier, Dominique / Favier, Roland / Duchamp, Claude / Desplanches, Dominique

Free radical biology & medicine

2007 Volume 42, Issue 5, Page(s) 627–635

Abstract: Exposure to reduced activity induces skeletal muscle atrophy. Oxidative stress might contribute to muscle wasting via proteolysis activation. This study aimed to test two hypotheses in rats. First, supplementation of the antioxidant vitamin E, prior and ... ...

Abstract	Exposure to reduced activity induces skeletal muscle atrophy. Oxidative stress might contribute to muscle wasting via proteolysis activation. This study aimed to test two hypotheses in rats. First, supplementation of the antioxidant vitamin E, prior and during the phase of unloading, would partly counteract unloading-induced soleus muscle atrophy. Secondly, vitamin E supplementation would decrease the rate of muscle proteolysis by reducing expression of calpains, caspases-3, -9, and -12, and E3 ubiquitin ligases (MuRF1 and MAFbx). Soleus muscle atrophy (-49%) induced by 14 days of hindlimb unloading was reduced to only 32% under vitamin E. Vitamin E partly prevented the decrease in type I and IIa fiber size. Supplementation increased HSP72 content and suppressed the rise in muscle level of thiobarbituric acid-reactive substance caused by unloading but failed to modify the lower ratio of reduced vs oxidized glutathione, the higher uncoupling proteins mRNA, and the antioxidant enzyme activities (superoxide dismutase, catalase, and glutathione peroxidase) observed after unloading. Vitamin E treatment abolished the large upregulation of caspases-9 and -12 and MuRF1 transcripts in unloaded muscle and greatly decreased the upregulation of mu-calpain, caspase-3, and MAFbx mRNA. In conclusion, the protective effect of vitamin E might be due to modulation of muscle proteolysis-related genes rather than to its antioxidant function.
MeSH term(s)	Animals ; Antioxidants/metabolism ; Dietary Supplements ; Gene Expression Regulation ; Glutathione/metabolism ; Hindlimb Suspension ; Lipid Peroxidation ; Male ; Muscle Fibers, Fast-Twitch/pathology ; Muscle, Skeletal/drug effects ; Muscle, Skeletal/pathology ; Muscular Atrophy/etiology ; Muscular Atrophy/pathology ; Muscular Atrophy/prevention & control ; Oxidation-Reduction ; Oxidative Stress/drug effects ; Oxidative Stress/physiology ; Protein Processing, Post-Translational ; Rats ; Rats, Wistar ; Vitamin E/administration & dosage ; Vitamin E/pharmacology
Chemical Substances	Antioxidants ; Vitamin E (1406-18-4) ; Glutathione (GAN16C9B8O)
Language	English
Publishing date	2007-03-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	807032-5
ISSN	1873-4596 ; 0891-5849
ISSN (online)	1873-4596
ISSN	0891-5849
DOI	10.1016/j.freeradbiomed.2006.12.001
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Article: Molecular system bioenergetics: regulation of substrate supply in response to heart energy demands.

Saks, Valdur / Favier, Roland / Guzun, Rita / Schlattner, Uwe / Wallimann, Theo

The Journal of physiology

2006 Volume 577, Issue Pt 3, Page(s) 769–777

Abstract: This review re-evaluates regulatory aspects of substrate supply in heart. In aerobic heart, the preferred substrates are always free fatty acids, and workload-induced increase in their oxidation is observed at unchanged global levels of ATP, ... ...

Abstract	This review re-evaluates regulatory aspects of substrate supply in heart. In aerobic heart, the preferred substrates are always free fatty acids, and workload-induced increase in their oxidation is observed at unchanged global levels of ATP, phosphocreatine and AMP. Here, we evaluate the mechanisms of regulation of substrate supply for mitochondrial respiration in muscle cells, and show that a system approach is useful also for revealing mechanisms of feedback signalling within the network of substrate oxidation and particularly for explaining the role of malonyl-CoA in regulation of fatty acid oxidation in cardiac muscle. This approach shows that a key regulator of fatty acid oxidation is the energy demand. Alterations in malonyl-CoA would not be the reason for, but rather the consequence of, the increased fatty acid oxidation at elevated workloads, when the level of acetyl-CoA decreases due to shifts in the kinetics of the Krebs cycle. This would make malonyl-CoA a feedback regulator that allows acyl-CoA entry into mitochondrial matrix space only when it is needed. Regulation of malonyl-CoA levels by AMPK does not seem to work as a master on-off switch, but rather as a modulator of fatty acid import.
MeSH term(s)	Animals ; Energy Metabolism ; Fatty Acids, Nonesterified/metabolism ; Glucose/metabolism ; Humans ; Muscle, Skeletal/metabolism ; Myocardium/metabolism ; Oxidation-Reduction
Chemical Substances	Fatty Acids, Nonesterified ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2006-12-15
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	3115-x
ISSN	1469-7793 ; 0022-3751
ISSN (online)	1469-7793
ISSN	0022-3751
DOI	10.1113/jphysiol.2006.120584
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Article ; Online: Inhibition of xanthine oxidase reduces hyperglycemia-induced oxidative stress and improves mitochondrial alterations in skeletal muscle of diabetic mice.

Bravard, Amélie / Bonnard, Charlotte / Durand, Annie / Chauvin, Marie-Agnès / Favier, Roland / Vidal, Hubert / Rieusset, Jennifer

American journal of physiology. Endocrinology and metabolism

2011 Volume 300, Issue 3, Page(s) E581–91

Abstract: Reactive oxygen species (ROS) have been widely implicated in the pathogenesis of diabetes and more recently in mitochondrial alterations in skeletal muscle of diabetic mice. However, so far the exact sources of ROS in skeletal muscle have remained ... ...

Abstract	Reactive oxygen species (ROS) have been widely implicated in the pathogenesis of diabetes and more recently in mitochondrial alterations in skeletal muscle of diabetic mice. However, so far the exact sources of ROS in skeletal muscle have remained elusive. Aiming at better understanding the causes of mitochondrial alterations in diabetic muscle, we designed this study to characterize the sites of ROS production in skeletal muscle of streptozotocin (STZ)-induced diabetic mice. Hyperglycemic STZ mice showed increased markers of systemic and muscular oxidative stress, as evidenced by increased circulating H(2)O(2) and muscle carbonylated protein levels. Interestingly, insulin treatment reduced hyperglycemia and improved systemic and muscular oxidative stress in STZ mice. We demonstrated that increased oxidative stress in muscle of STZ mice is associated with an increase of xanthine oxidase (XO) expression and activity and is mediated by an induction of H(2)O(2) production by both mitochondria and XO. Finally, treatment of STZ mice, as well as high-fat and high-sucrose diet-fed mice, with oxypurinol reduced markers of systemic and muscular oxidative stress and prevented structural and functional mitochondrial alterations, confirming the in vivo relevance of XO in ROS production in diabetic mice. These data indicate that mitochondria and XO are the major sources of hyperglycemia-induced ROS production in skeletal muscle and that the inhibition of XO reduces oxidative stress and improves mitochondrial alterations in diabetic muscle.
MeSH term(s)	Adenosine Triphosphate/biosynthesis ; Animals ; Antioxidants/metabolism ; Diabetes Mellitus, Experimental/enzymology ; Diabetes Mellitus, Experimental/metabolism ; Diabetes Mellitus, Type 1/chemically induced ; Diabetes Mellitus, Type 1/metabolism ; Diabetes Mellitus, Type 2/chemically induced ; Diabetes Mellitus, Type 2/metabolism ; Diet ; Enzyme Inhibitors/pharmacology ; Hydrogen Peroxide/metabolism ; Hyperglycemia/complications ; Insulin/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Microscopy, Electron, Transmission ; Mitochondria, Muscle/enzymology ; Mitochondria, Muscle/physiology ; Muscle, Skeletal/enzymology ; Muscle, Skeletal/metabolism ; Oxidative Stress/physiology ; Oxypurinol/pharmacology ; Protein Carbonylation/drug effects ; RNA/genetics ; Reverse Transcriptase Polymerase Chain Reaction ; Xanthine Oxidase/antagonists & inhibitors
Chemical Substances	Antioxidants ; Enzyme Inhibitors ; Insulin ; RNA (63231-63-0) ; Adenosine Triphosphate (8L70Q75FXE) ; Hydrogen Peroxide (BBX060AN9V) ; Xanthine Oxidase (EC 1.17.3.2) ; Oxypurinol (G97OZE5068)
Language	English
Publishing date	2011-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	603841-4
ISSN	1522-1555 ; 0193-1849
ISSN (online)	1522-1555
ISSN	0193-1849
DOI	10.1152/ajpendo.00455.2010
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Article: High Expression of Thyroid Hormone Receptors and Mitochondrial Glycerol-3-phosphate Dehydrogenase in the Liver Is Linked to Enhanced Fatty Acid Oxidation in Lou/C, a Rat Strain Resistant to Obesity

Taleux, Nellie / Guigas, Bruno / Dubouchaud, Hervé / Moreno, Maria / Weitzel, Joachim M / Goglia, Fernando / Favier, Roland / Leverve, Xavier M

Journal of biological chemistry. 2009 Feb. 13, v. 284, no. 7

2009

Abstract: Besides its well recognized role in lipid and carbohydrate metabolisms, glycerol is involved in the regulation of cellular energy homeostasis via glycerol-3-phosphate, a key metabolite in the translocation of reducing power across the mitochondrial inner ...

Abstract	Besides its well recognized role in lipid and carbohydrate metabolisms, glycerol is involved in the regulation of cellular energy homeostasis via glycerol-3-phosphate, a key metabolite in the translocation of reducing power across the mitochondrial inner membrane with mitochondrial glycerol-3-phosphate dehydrogenase. Here, we report a high rate of gluconeogenesis from glycerol and fatty acid oxidation in hepatocytes from Lou/C, a peculiar rat strain derived from Wistar, which is resistant to age- and diet-related obesity. This feature, associated with elevated cellular respiration and cytosolic ATP/ADP and NAD⁺/NADH ratios, was linked to a high expression and activity of mitochondrial glycerol-3-phosphate dehydrogenase. Interestingly, this strain exhibited high expression and protein content of thyroid hormone receptor, whereas circulating thyroid hormone levels were slightly decreased and hepatic thyroid hormone carrier MCT-8 mRNA levels were not modified. We propose that an enhanced liver thyroid hormone receptor in Lou/C may explain its unique resistance to obesity by increasing fatty acid oxidation and lowering liver oxidative phosphorylation stoichiometry at the translocation of reducing power into mitochondria.
Language	English
Dates of publication	2009-0213
Size	p. 4308-4316.
Publishing place	American Society for Biochemistry and Molecular Biology
Document type	Article
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
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Article: High expression of thyroid hormone receptors and mitochondrial glycerol-3-phosphate dehydrogenase in the liver is linked to enhanced fatty acid oxidation in Lou/C, a rat strain resistant to obesity.

Taleux, Nellie / Guigas, Bruno / Dubouchaud, Hervé / Moreno, Maria / Weitzel, Joachim M / Goglia, Fernando / Favier, Roland / Leverve, Xavier M

The Journal of biological chemistry

2008 Volume 284, Issue 7, Page(s) 4308–4316

Abstract	Besides its well recognized role in lipid and carbohydrate metabolisms, glycerol is involved in the regulation of cellular energy homeostasis via glycerol-3-phosphate, a key metabolite in the translocation of reducing power across the mitochondrial inner membrane with mitochondrial glycerol-3-phosphate dehydrogenase. Here, we report a high rate of gluconeogenesis from glycerol and fatty acid oxidation in hepatocytes from Lou/C, a peculiar rat strain derived from Wistar, which is resistant to age- and diet-related obesity. This feature, associated with elevated cellular respiration and cytosolic ATP/ADP and NAD(+)/NADH ratios, was linked to a high expression and activity of mitochondrial glycerol-3-phosphate dehydrogenase. Interestingly, this strain exhibited high expression and protein content of thyroid hormone receptor, whereas circulating thyroid hormone levels were slightly decreased and hepatic thyroid hormone carrier MCT-8 mRNA levels were not modified. We propose that an enhanced liver thyroid hormone receptor in Lou/C may explain its unique resistance to obesity by increasing fatty acid oxidation and lowering liver oxidative phosphorylation stoichiometry at the translocation of reducing power into mitochondria.
MeSH term(s)	Adenosine Diphosphate/metabolism ; Adenosine Triphosphate/metabolism ; Animals ; Fatty Acids/metabolism ; Gluconeogenesis/physiology ; Glycerol/metabolism ; Glycerolphosphate Dehydrogenase/metabolism ; Glycerophosphates/metabolism ; Hepatocytes/metabolism ; Male ; Mitochondria, Liver/metabolism ; Monocarboxylic Acid Transporters ; NAD/metabolism ; Obesity ; Oxidation-Reduction ; Rats ; Rats, Wistar ; Receptors, Thyroid Hormone/metabolism ; Species Specificity
Chemical Substances	Fatty Acids ; Glycerophosphates ; Monocarboxylic Acid Transporters ; Receptors, Thyroid Hormone ; monocarboxylate transporter 8, rat ; NAD (0U46U6E8UK) ; Adenosine Diphosphate (61D2G4IYVH) ; Adenosine Triphosphate (8L70Q75FXE) ; Glycerolphosphate Dehydrogenase (EC 1.1.-) ; Glycerol (PDC6A3C0OX)
Language	English
Publishing date	2008-12-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.M806187200
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Article: Mitochondrial adaptations to steatohepatitis induced by a methionine- and choline-deficient diet.

Romestaing, Caroline / Piquet, Marie-Astrid / Letexier, Dominique / Rey, Benjamin / Mourier, Arnaud / Servais, Stéphane / Belouze, Maud / Rouleau, Vincent / Dautresme, Marianne / Ollivier, Isabelle / Favier, Roland / Rigoulet, Michel / Duchamp, Claude / Sibille, Brigitte

American journal of physiology. Endocrinology and metabolism

2008 Volume 294, Issue 1, Page(s) E110–9

Abstract: Nonalcoholic fatty liver disease (NAFLD) has become common liver disease in Western countries. There is accumulating evidence that mitochondria play a key role in NAFLD. Nevertheless, the mitochondrial consequences of steatohepatitis are still unknown. ... ...

Abstract	Nonalcoholic fatty liver disease (NAFLD) has become common liver disease in Western countries. There is accumulating evidence that mitochondria play a key role in NAFLD. Nevertheless, the mitochondrial consequences of steatohepatitis are still unknown. The bioenergetic changes induced in a methionine- and choline-deficient diet (MCDD) model of steatohepatitis were studied in rats. Liver mitochondria from MCDD rats exhibited a higher rate of oxidative phosphorylation with various substrates, a rise in cytochrome oxidase (COX) activity, and an increased content in cytochrome aa3. This higher oxidative activity was associated with a low efficiency of the oxidative phosphorylation (ATP/O, i.e., number of ATP synthesized/natom O consumed). Addition of a low concentration of cyanide, a specific COX inhibitor, restored the efficiency of mitochondria from MCDD rats back to the control level. Furthermore, the relation between respiratory rate and protonmotive force (in the nonphosphorylating state) was shifted to the left in mitochondria from MCDD rats, with or without cyanide. These results indicated that, in MCDD rats, mitochondrial ATP synthesis efficiency was decreased in relation to both proton pump slipping at the COX level and increased proton leak although the relative contribution of each phenomenon could not be discriminated. MCDD mitochondria also showed a low reactive oxygen species production and a high lipid oxidation potential. We conclude that, in MCDD-fed rats, liver mitochondria exhibit an energy wastage that may contribute to limit steatosis and oxidative stress in this model of steatohepatitis.
MeSH term(s)	Adaptation, Physiological/physiology ; Animal Feed ; Animals ; Choline/pharmacology ; Choline Deficiency/metabolism ; Choline Deficiency/physiopathology ; Energy Metabolism/physiology ; Fatty Liver/metabolism ; Fatty Liver/physiopathology ; Hepatitis/metabolism ; Hepatitis/physiopathology ; Interleukin-6/genetics ; Male ; Malnutrition/metabolism ; Malnutrition/physiopathology ; Methionine/deficiency ; Methionine/pharmacology ; Mitochondria, Liver/metabolism ; Oxidative Phosphorylation ; Oxygen Consumption/physiology ; Rats ; Rats, Wistar ; Receptors, Tumor Necrosis Factor/genetics ; Reverse Transcriptase Polymerase Chain Reaction ; Tumor Necrosis Factor-alpha/genetics
Chemical Substances	Interleukin-6 ; Receptors, Tumor Necrosis Factor ; Tumor Necrosis Factor-alpha ; Methionine (AE28F7PNPL) ; Choline (N91BDP6H0X)
Language	English
Publishing date	2008-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	603841-4
ISSN	1522-1555 ; 0193-1849
ISSN (online)	1522-1555
ISSN	0193-1849
DOI	10.1152/ajpendo.00407.2007
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Article: Dopaminergic metabolism in carotid bodies and high-altitude acclimatization in female rats.

Joseph, Vincent / Soliz, Jorge / Soria, Ruddy / Pequignot, Jacqueline / Favier, Roland / Spielvogel, Hilde / Pequignot, Jean Marc

American journal of physiology. Regulatory, integrative and comparative physiology

2002 Volume 282, Issue 3, Page(s) R765–73

Abstract: We tested the hypothesis that ovarian steroids stimulate breathing through a dopaminergic mechanism in the carotid bodies. In ovariectomized female rats raised at sea level, domperidone, a peripheral D2-receptor antagonist, increased ventilation in ... ...

Abstract	We tested the hypothesis that ovarian steroids stimulate breathing through a dopaminergic mechanism in the carotid bodies. In ovariectomized female rats raised at sea level, domperidone, a peripheral D2-receptor antagonist, increased ventilation in normoxia (minute ventilation = +55%) and acute hypoxia (+32%). This effect disappeared after 10 daily injections of ovarian steroids (progesterone + estradiol). At high altitude (3,600 m, Bolivian Institute for High-Altitude Biology-IBBA, La Paz, Bolivia), neutered females had higher carotid body tyrosine hydroxylase activity (the rate-limiting enzyme for catecholamine synthesis: +129%) and dopamine utilization (+150%), lower minute ventilation (-30%) and hypoxic ventilatory response (-57%), and higher hematocrit (+18%) and Hb concentration (+21%) than intact female rats. Consistent signs of arterial pulmonary hypertension (right ventricular hypertrophy) also appeared in ovariectomized females. None of these parameters was affected by gonadectomy in males. Our results show that ovarian steroids stimulate breathing by lowering a peripheral dopaminergic inhibitory drive. This process may partially explain the deacclimatization of postmenopausal women at high altitude.
MeSH term(s)	Acclimatization/physiology ; Altitude ; Animals ; Cardiomegaly/etiology ; Carotid Body/drug effects ; Carotid Body/metabolism ; Catecholamines/metabolism ; Domperidone/pharmacology ; Dopamine/metabolism ; Estradiol/pharmacology ; Female ; Hematocrit ; Hemoglobins/analysis ; Hypoxia/physiopathology ; Male ; Ovariectomy ; Progesterone/pharmacology ; Rats ; Rats, Sprague-Dawley ; Respiration/drug effects ; Rest
Chemical Substances	Catecholamines ; Hemoglobins ; Progesterone (4G7DS2Q64Y) ; Estradiol (4TI98Z838E) ; Domperidone (5587267Z69) ; Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2002-01-29
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	603839-6
ISSN	1522-1490 ; 0363-6119
ISSN (online)	1522-1490
ISSN	0363-6119
DOI	10.1152/ajpregu.00398.2001
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In stock of ZB MED Cologne/Königswinter

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Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito